STOCKHOLM — Autoantibodies directed against the β1-adrenergic receptor appear to play a role in the pathogenesis of postpartum cardiomyopathy, Gerd Wallukat, M.D., said at the annual congress of the European Society of Cardiology.
Evidence has implicated autoantibodies against the β1-adrenergic receptor in the development of dilated cardiomyopathy. In light of that, Dr. Wallukat and coworkers sought evidence of a similar phenomenon in 26 women with postpartum cardiomyopathy.
They found it. Serum obtained when the women presented in New York Heart Association functional class III or IV with postpartum cardiomyopathy did show such autoantibodies in all 26 patients and in none of a healthy age-matched control group. The autoantibodies appeared to have a dose-dependent agonist effect, said Dr. Wallukat of the Max Delbrück Center, Berlin.
The autoantibodies were identified using a bioassay that utilized cultured, spontaneously beating, neonatal rat cardiomyocytes, which beat faster on β-adrenergic stimulation. Prolonged exposure did not desensitize the β1-adrenergic receptors.
The agonist effect was inhibited in vitro by β1-adrenergic receptor antagonists, which explains the improvement of postpartum cardiomyopathy patients when treated with β-blockers.
Sera obtained after 6 months showed a sharp reduction in autoantibody activity. This improvement was paralleled in the New York Heart Association functional class and cardiac function in 24 of the 26 women.